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Myasthenia

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Part of the book series: Current Histopathology ((CUHI,volume 9))

Abstract

Myasthenia gravis (MG) is now well established as an autoimmune disease mediated by antibodies to acetylcholine receptors which initiate structural damage to the motor end plate. Simplification of the normally complex junctional folds of the end plate correlates with defective neuromuscular transmission (Figures 7.1–7.3, Diagrams 7.1 and 7.2). There is a distinctive clinical picture of increased fatiguability and temporary muscle weakness. Initial symptoms are often ptosis, diplopia or blurring of vision, due to involvement of the extra-ocular muscles. In the majority of patients the disease soon becomes generalized, affecting speech and swallowing as well as limb muscles1. Sometimes there is severe bulbar weakness with sparing of limb muscles. The most severe generalized disease involves the respiratory muscles, increasing susceptibility to chest infection. In approximately 20% of patients, clinical manifestations remain limited to the extra-ocular muscles, although EMG investigation will reveal more widespread abnormalities. It is suggested that if the disease has been localized for a year, further progression is unlikely1. In chronic disease temporary muscle weakness may give way to persistent weakness, accompanied by atrophy. In all patients symptoms tend to fluctuate.

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© 1985 Janice R. Anderson

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Anderson, J.R. (1985). Myasthenia. In: Atlas of Skeletal Muscle Pathology. Current Histopathology, vol 9. Springer, Dordrecht. https://doi.org/10.1007/978-94-009-4866-2_7

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  • DOI: https://doi.org/10.1007/978-94-009-4866-2_7

  • Publisher Name: Springer, Dordrecht

  • Print ISBN: 978-94-010-8653-0

  • Online ISBN: 978-94-009-4866-2

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